Scientists discover the 'key' to preventing hair from turning grey

Graying of hair tends to happen as we age, which makes many think that it is a major factor in aging without actually thinking about the process that causes it.

Scientists now believe they have discovered the mechanism of hair turning grey, which could help develop a cell-altering treatment to reverse or stop the process.

The new study suggests that as hair ages, stem cells may falter and lose their ability to mature and maintain hair color.

Some stem cells (cells capable of developing into many different cell types) have the unique ability to move between the growth chambers of a hair follicle.

It is these cells that lose the ability to move with age, paving the way for graying of hair.

Led by researchers from New York University Grossman School of Medicine, the research focused on cells found in the skin of mice and also found in humans called melanoma stem cells, or McSC.

The scientists suggested that if their findings hold true for humans, it could open up a potential way to reverse or prevent hair graying.

And hair color is controlled by whether the ongoing proliferation of McSC clusters within the hair follicle (from where hair grows) get a signal to become mature cells that make the protein pigments responsible for color.

Scientists found that during normal hair growth, these cells constantly move back and forth as they travel between the chambers of the growing hair follicle.

Within these compartments, melanoma stem cells (McSCs) are exposed to signals that affect maturation.

Specifically, the research team found that melanoma stem cells switch between a more primitive stem cell state and the next stage of their maturation, the transit-amplifying state, depending on their location.

According to the findings, as hair ages, falls out, and then grows back repeatedly, increasing numbers of melanoma stem cells get stuck in a part of the stem cells called the hair follicle bulge (or hair follicle bump).

They remain there and do not mature to the transitory amplification state, and do not migrate back to their original location in the chamber, where they would have been induced to regenerate into the melanocytes.

"Our study adds to our fundamental understanding of how melanocyte stem cells color hair," said the study's principal investigator, Qi San, a postdoctoral fellow at NYU Langone Health. "The newly discovered mechanisms raise the possibility that there is the same fixed placement of stem cells for melanocytes in humans." If so, it represents a potential pathway to reverse or prevent graying of human hair by helping the stacked cells move back between the chambers of the growing hair follicles."

In experiments with mice whose hair had been physically aged by plucking and forced regrowth, the number of hair follicles containing melanoma stem cells (McSC) present in the follicle bulge increased from 15% before plucking to almost half after forced aging.

The study, published in the journal Nature, found that these cells remained unable to regenerate or mature into pigment-producing melanocytes.

The scientists found that the stuck CSCs stopped their regenerative behavior as they were no longer exposed to many of the signals that allowed them to produce pigment in the new hair follicles, which continued to grow.

But other melanoma stem cells that continued to move back and forth between the bulge of the follicles (follicle) retained their ability to regenerate while the melanocytes matured and produced pigment over the two-year study period.

How long can a person live? The answer may surprise you!

The world's richest people, such as Larry Page, Mark Zuckerberg, and Jeff Bezos, have invested huge sums in biotechnology companies that seek to extend life through cell regeneration and disease prevention.

To date, the longest anyone has clung on in their lifetime is 122 years. But that may be on the lower end of the potential.

Human life may reach 150 years

Even if you lived in a bubble free of disease or danger, your body would still experience wear and tear as it pumped blood, digested food, and performed all the functions needed to survive.

And the older you get, the longer your body takes to "bounce back" from this wear and tear, because aging seeps into our cells and DNA. All of this means that your tissues gradually lose their ability to heal themselves, which can lead to disease and dysfunction.

Here, one study suggested that the human body's recovery time doubles every 15 years - so a bruise that takes a week to heal at age 40 might take two weeks at age 55. Eventually, the human body loses all its elasticity, and once many parts of the body fail, they die.

And researchers don't necessarily agree on the maximum time for this to happen. Some suggested 115 years, others suggested 130 years.

One of the most recent studies, which analyzed more than half a million people in the United States and the United Kingdom, indicated that humans lose all flexibility sometime between the ages of 120-150.

The big question becomes: What if we could slow this wear and tear, or better yet, prevent it altogether? Some experts argue that with medical advances, human life expectancy has no natural limits.

Let's take a look at aging at the cellular level, what's holding us back from living longer, and at groups of researchers looking to understand and possibly reverse the aging process.

Cellular aging is one of the most researched aging topics

Cellular senescence occurs when a cell stops reproducing but does not die.

When this happens, some of the senescent cells turn into destructive zombies, floating around and releasing inflammatory chemicals that damage healthy cells, including stem cells - the body's "repairmen" that help replace damaged tissue. But not all senescent cells are bad.

Some senescent cells secrete chemicals that help repair wounds, said Paul Robbins, associate director of the Institute of Aging Biology and Metabolism and the Biology of Aging Medical Discovery Group at the University of Minnesota.

Companies such as Life Biosciences and Unity Biotechnology are currently developing drugs called senolytics to contain and destroy only the "bad" senescent cells in your body. Some experimental drugs may even prevent cells from becoming senescent in the first place.

But so far, no one has figured out how to prevent or completely eliminate harmful senescent cells.

By the age of 60, Robbins said, the human body — particularly the immune system — has a more difficult time getting rid of harmful aging cells, which can lead to a buildup that leads to tissue damage and failure. One of the main causes of cellular aging is damage to your DNA, which helped launch another area of ​​research that led to a Nobel Prize in 2009: telomeres.

Telomeres help estimate your biological age

Some argue that biological age — how old your cells and tissues are — is a better predictor of life span than your chronological age, or the number of years you've been alive.

A common way that scientists estimate biological age is by measuring telomeres in specific immune cells. Telomeres are the protective caps at the end of your DNA. They are made up of chains of molecules called base pairs. As you age, these base pairs disappear, causing your telomeres to shorten. Shorter telomeres also make DNA more susceptible to damage and the effects of aging.

When born, telomeres in certain immune cells, called leukocytes, can contain between 7,000 and 11,600 base pairs. And a recent study found that once that size shrinks to 5,000 bp, you're at imminent risk of death.

But other research has found that some people over the age of 100 actually have telomeres that get longer every year, not shorter. This has led some scientists to look for ways to mimic the telomere recovery process in younger individuals.

For example, Clinics Aviv conducted a study examining how 35 elderly adults responded to hyperbaric oxygen therapy, where they rest in a room with high air pressure and oxygen levels. They were able to increase the telomere length in the white blood cells of the participants after 30 daily HBOT sessions.

But most of the telomeres stopped growing after the 30th session, and scientists don't yet know how long the effects of the treatment might last.

DNA methylation is associated with several age-related diseases

Another factor that contributes to DNA damage and cellular aging is DNA methylation — when molecules called methyl groups attach to specific sections of your genes to manage their behavior.

Depending on the site, methyl groups may prevent genes from activating or enhance gene activity when necessary.

In general, DNA methylation decreases as you age, which may allow faulty genes to be activated.

Research has linked reduced methylation to several age-related conditions, including Alzheimer's disease, cardiovascular disease and cancer — although it's worth noting that not all methylation changes are bad.

Similar to telomeres, DNA methylation is another way scientists can measure your biological age to help predict your life expectancy. For example, you may have celebrated your 55th birthday, but after years of smoking, your cells may have a level of methylation typically seen in people over 60, leading to a shortened lifespan.

Traditionally, DNA methylation tests have used blood, but companies such as Elysium Health and research projects such as GrimAge have recently developed saliva tests as well.

Research found that people who were at least five years more methylated than their chronological age had a 16% higher risk of mortality, meaning they were more likely to die from any cause than their peers of the same age.

Mitochondria and free radicals are among the biggest obstacles to longevity

Last but not least, some of the biggest determinants of human lifespan are the tiny, bean-shaped mitochondria in your cells. These microscopic structures generate most of the cell's energy, which is vital for survival, but they also create byproducts called free radicals, which are essentially unstable atoms that bounce around and harm parts of your cell, leading to damage called oxidative stress. Over time, oxidative stress builds up, causing age-related diseases such as Parkinson's, Alzheimer's and cancer.

Biotechnology companies such as Altos Labs are working on a way to prevent these diseases by regenerating cells and undoing the damage that oxidative stress can cause. The company hopes that by returning cells to a healthier, more youthful state, this can lead to increased longevity.

The pursuit of longevity has no single solution

There are groups of people working to understand and possibly reverse these processes. But it is important to note that the aging puzzle does not have a single solution.

"All of these things that get worse with age are related," Robbins said.

For example, telomere shortening can lead to DNA damage, which in turn disrupts mitochondria. Free radicals from mitochondria can, in turn, damage more telomeres and DNA. All these processes mutually affect each other.

No aging mechanism is more important than the other elements. This is why all anti-aging research, no matter how specialized, is a continuum of humanity's larger goal: to stay alive as long as possible.